PRESSOR AND REFLEX SENSITIVITY IS ALTERED IN SPONTANEOUSLY HYPERTENSIVE RATS TREATED WITH ANGIOTENSIN-(1-7)

We have suggested that angiotensin-(1-7) [Ang(1-7)] may oppose the pre sser activity of angiotensin II (Ang II). This hypothesis was supporte d by the fact that long-term intravenous infusion of Ang-(1-7) transie ntly lowers blood pressure in spontaneously hypertensive rats (SHR). W e now investigated whether the presser sensitivity to bolus injections of either phenylephrine (PE) or Ang II was altered on day 12 of an An g-(1-7) infusion when blood pressure in the SHR had returned to hypert ensive levels. SHR (n=10) and WKY rats (n=8) were given Ang-(1-7) intr avenously via osmotic minipumps at a dose of 24 mu g/kg per hour for 2 weeks. On day 12 of the infusion, mean arterial pressure and heart ra te in halothane-anesthetized rats were similar in Ang-(1-7)-treated SH R (142+/-6 mm Hg; 388+/-9 beats per minute) and those infused with veh icle (146+/-5 mm Hg; 392+/-13 beats per minute). Presser responsivenes s to PE in Ang-(1-7)-treated SHR was 22% less at a dose of 10 mu g, wh ile presser responses to Ang II decreased by 20% and 25% at doses of 0 .05 and 0.1 mu g, respectively, compared with the vehicle-treated SHR (P<.O5). There were no effects of the Ang-(1-7) infusion on presser re sponses to Ang II or PE in WKY rats. In the SHR infused with Ang-(1-7) , there was a 35% improvement in sensitivity of the reflex control of heart rate to levels not different from those in the untreated WKY rat s (slope of the change in pulse interval versus the change in pressure increased from 0.34+/-0.03 to 0.46+/-0.01 ms/mm Hg). These data sugge st that Ang-(1-7) may selectively activate antihypertensive mechanisms at the level of the vascular wall or the baroreflex.